摘要
血运重建是目前治疗心肌缺血的最有效方法,但治疗过程中,缺血区域的再灌注加速诱导受损心肌细胞的凋亡,加重心肌缺血、缺氧,导致心肌缺血再灌注损伤(MIRI)。NADPH氧化酶2(Nox2)生成活性氧(ROS)诱导氧化应激引起心肌氧化损伤。ATP敏感性钾通道(KATP)通过调节MIRI期间能量消耗、减少缺血再灌注心肌细胞ROS的产生,发挥心脏保护的重要作用。本文综述了Nox2和KATP介导MIRI的近期研究进展,同时探究了缺血再灌注心肌细胞中KATP对Nox2的调控作用。
Revascularization is currently the most effective method for the treatment of myocardial ischemia.However,in the process of treatment,reperfusion of ischemic area accelerates the apoptosis of damaged cardiomyocytes,aggravates myocardial ischemia and hypoxia,and leads to myocardial ischemia reperfusion injury(MIRI).NADPH oxidase-2(Nox2)generates reactive oxygen species(ROS)to induce oxidative stress and cause myocardial oxidative damage.ATP-sensitive potassium channel(KATP)plays an important role in cardiac protection by regulating energy consumption during MIRI and reducing ROS production in myocardial cells after ischemia reperfusion.This article reviews the recent research progress of Nox2 and KATP mediated MIRI,and explores the regulatory role of KATP on Nox2 in ischemia reperfusion cardiomyocytes.
作者
郭茹
蔺雪峰
李阳
聂晓丽
韩轩茂
GUO Ru;LIN Xuefeng;LI Yang;NIE Xiaoli;HAN Xuanmao(Graduate School,Baotou Medical College,First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou,Inner Mongolia 014040,China;Department of Cardiology,First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou,Inner Mongolia 014040,China)
出处
《中国动脉硬化杂志》
CAS
2021年第8期725-731,共7页
Chinese Journal of Arteriosclerosis
基金
内蒙古自治区自然科学基金(2016MS08101)
包头医学院科学研究基金(BYJJ-QM-2018021)。
